Acclimatization allows permanent residents at high altitudes to adjust to low oxygen levels through various compensatory mechanisms. These include increased pulmonary ventilation, higher red blood cell counts and hemoglobin concentration, decreased oxygen affinity of hemoglobin, and enhanced diffusion capacity. At the tissue level, capillarity increases and cellular changes improve oxygen utilization. Natives born at high altitude exhibit superior acclimatization through enhanced lung size, heart adaptations, and optimized oxygen delivery and transport. Failure to acclimatize can result in acute or chronic mountain sickness without appropriate ascent rates or remaining at altitude too long.

1. Acclimatization
(to low Oxygen at high altitude)
Pandian M
Dept. of Physiology

2. • Introduction to Physiology of High Altitude
• Fall in barometric pressure
• Hazards of rapid ascent.
• ‘Safe Zone’ of ascent.
• Upto 12,000 feet- CVS & RS involvement.

3. Definition :- Readjustments & compensatory
mechanism which takes place in the body to
reduce the effects of hypoxia in those persons
(permanent residents) at high altitude is called
acclimatization at high altitude.
This makes possible for the permanent
residents there to lead a normal & prolonged
life, work harder without hypoxic effects or
to ascend to still higher altitude.

4. Acclimatization is possible by following
process
1. Increase in pulmonary ventilation.
2. Decrease affinity of Hb for O2 under hypoxic
condition.
3. Rise in Hb Conc.
4. Increases vascularity of hypoxic tissues.
5. Increased diffusion capacity of lungs for O2
6. Changes at tissue level to reduced the effect
of hypoxia

5. unacclimatized
• At sea level, normal arterial pO2 and pCO2 are 100 to
40 mmHg.
• When rapid ascend in unacclimatized subjects, upto
10,000 ft ↓ses arterial pO2 to 60 mmHg while pCO2 is
kept normal.
• So, no ↑s in pul.vent.
• But, after 10,000ft art.pCO2 falls rapidly due to ↑s in
pul.ventilation.

6. Acclimatized
• Sensitivity of Resp.center ↑sed.(hypoxia)
• even, slightly ↓se of art.pO2, causes pulm.
Vent. ↑ses and alveolar pCO2 falls.
• This ↑ se in pul.vent is maintained by active
regulation of pH of CSF & blood to normal
levels.??

7. • Active transport of HCO-
3 out of CSF or
• Active transport of H+ into CSF or
• Hypoxia causes LA formation this ↑ses H+
Conc.

8. CHANGES DURING ACCLIMATIZATION
• Various changes that take place during
acclimatization
• help the body to cope with adverse effects
of hypoxia at high altitude.
1. Changes in Blood
2. Changes in Cardiovascular System
3. Changes in Respiratory System
4. Changes in Tissues

9. Compensatory mechanisms
1) ↑ in pulmonary ventilation.
2) ↑ in red blood cell count.
3) ↑ in hemoglobin concentration.
4) ↑ in blood volume.
5) ↓ affinity of the hemoglobin for O2.
6) ↑ diffusing capacity.
7) ↑ capillarity.
8) Cellular acclimatization (change at tissue level).
9) Natural acclimatization of natives living at high altitude.

10. 1) ↑ in pulmonary ventilation
At high altitude barometric pressure ↓
↓
↓ partial pressure of O2
↓
↓ alveolar Po2
↓
↓ arterial Po2
↓
Stimulation of arterial chemoreceptors

11.  Immediate effect i.e. in sec there is ↑
alveolar ventilation by 1.65 times normal.
 But after acclimatization it ↑ by 5 times
normal (400% above normal).
 Basic cause for ↑ pulmonary ventilation is
regulation of PH of CSF & blood by kidneys.

12.  ↑ pulmonary ventilation → CO2 wash out →
alkalosis which inhibits respiration.
 But kidneys actively excretes large amount of
HCO3
-
in urine & maintains blood PH to normal.
 So the inhibitory effect due to CO2 wash out
fades away
This effect of Co2 on resp. cent. Is potent for 1st
few hours (1 to 2 days)
 Respiratory centers responds to full force to the
peripheral chemoreceptors stimuli due to hypoxia.

13. 2) ↑ RBC count
• Hypoxia acts as powerful stimulant for erythropoietin
secretion → erythropoisis starts in 2 weeks.
• ↑ in RBC count from 5.5 millions/ cumm to 7-8
millions/ cumm of blood.
• ↑ in Hb concentration from 15gm % to 20 gm %.
• ↑ in Haematocrit value from 45 % to 60 %.
• ↑ in blood volume by 20 to 30 %→↑ in circulating Hb
to 50 %.
• This results in ↑ O2 carrying capacity of blood.

14. 3) ↓ affinity of the Hb for O2
-Hypoxia leads to ↑ 2-3 DPG in RBCs.
- 2-3 DPG has high affinity for Hb.
- It shifts the O2 Hb dissociation curve to right
by displacing O2 from its sites.
- So more release of O2 from Hb to the tissues.

15. 4) ↑ Diffusing capacity through pulmonary membrane
• Normal diffusing capacity of O2 is 21ml/mm of Hg/min.
It ↑ by three fold, cause are;
i) ↑ pulmonary capillary blood volume → expands
the capillaries → ↑ surface area for diffusion.
ii) ↑ in lung volume → ↑ surface area of the
alveolar membrane.
iii) ↑ pulmonary arterial pressure → more blood
into more number of alveolar capillaries
(opening of more pulmonary capillaries)
especially in upper parts of lungs. So ideal
ventilation perfusion ratio.

16. 5) ↑ Capillarity
• Immediately after ascending high altitude there is ↑
cardiac output. But as blood haematocrit value ↑
cardiac output becomes normal.
• Another change is ↑ in number of systemic
capillaries (i.e. in non pulmonary tissues).
• This effect seen much in the tissues of animals born
& breed at high altitude, but to less extent in those
who are exposed to high altitude later in life.
• ↑ capillarity seen in Rt ventricle muscle due to
combined effect of hypoxia & excess work load on Rt
ventricle caused by pulmonary hypertension.

17. 6) Cellular acclimatization
• In natives changes occur at tissue level to reduce
the effect of hypoxia.
1)↑ Cell mitochondria (sites of oxidative reactions).
2)↑ in Oxidative enzyme systems e.g. cytochrome
oxidase.
3)↑ in synthesis of myoglobin (O2 storing pigment).
Thus the cells of acclimatized humans can use O2
more effectively.

18. 7) Natural acclimatization
Those persons born & live at high altitude all their
life shows certain changes in their bodies which
begin at infancy.
i) Chest size is greatly ↑ where as body size some
what ↓. This gives high ratio of ventilatory capacity
to body mass.
ii) Their hearts (particularly Rt side) provides high
pulmonary arterial pressures to pump blood through
greatly expanded pulmonary capillary system.
Hence Rt side heart larger than that of low landers.

19. iii) Delivery of O2 by the blood to the tissues is
highly facilitated. Arterial Po2 is only 40 mm of Hg
but due to ↑ conc. of Hb, the O2 content of blood is
more.
 Venous Po2 is 25mm of Hg i.e. only 15 mm of
Hg less than low landers (40 mm of Hg).
 This indicates O2 transport to the tissues is
exceedingly effective in the naturally acclimatized
persons. Thus natives are superior than best
acclimatized low landers.

20. Applied
 Acute mountain sickness
 Chronic mountain sickness

21. Acute mountain sickness
Due to rapid ascent & it leads to over reaction
1.Acute cerebral edema –vasodilation due to hypoxia
2.Acute pulmonary edema – increased pulmonary
pressure leads to accumulation of fluid in some
alveoli.
Treatment:- Oxygen & remove to a low altitude.

22. Chronic mountain sickness
• Develop in a person who remains at high altitude for
too long duration.
• Effects are;
- RBC and haematocrit becomes very high.
- Pulm. Arterial pressure becomes elevated.
- Right side of the heart becomes hypertrophied.
- Peripheral arterial pressure begins to fall.
- CCF occurs.
- Death.
Treatment:- Move to a low altitude.

23. THANK YOU . . .